Studies of embryo transfer from cattle clinically affected by bovine spongiform encephalopathy (BSE)

Abstract

Semen from 13 bulls, eight with clinical bovine spongiform encephalopathy (BSE), was used to artificially inseminate (AI) 167 cows with clinical BSE, and their resultant embryos were collected non-surgically seven days after AI. The viable and non-viable embryos with intact zonae pellucidae were washed 10 times (as recommended by the International Embryo Transfer Society) then frozen. Later, 587 of the viable embryos were transferred singly into 347 recipient heifers imported from New Zealand, and 266 live offspring were born of which 54.1 per cent had a BSE-positive sire and a BSE-positive dam. The recipients were monitored for clinical signs of BSE for seven years after the transfer, and the offspring were monitored for seven years after birth. Twenty-seven of the recipients and 20 offspring died while being monitored but none showed signs of BSE. Their brains, and the brains of the recipients and offspring killed after seven years, were examined for BSE by histopathology, PrP immunohistochemistry, and by electron microscopy for scrapie-associated fibrils. They were all negative. In addition, 1020 non-viable embryos were sonicated and injected intracerebrally into susceptible mice (20 embryos per mouse) which were monitored for up to 700 days, after which their brains were examined for spongiform lesions. They were all negative. It is concluded that embryos are unlikely to carry BSE infectivity even if they have been collected at the end-stage of the disease, when the risk of maternal transmission is believed to be highest.

TSE pathogenesis in cattle and sheep

“…In BSE of cattle all the evidence indicates that under natural conditions the BSE agent does not spread horizontally into the environment by any secreta or excreta or vertically through maternal transmission; in other words for BSE cattle are a dead-end host [12,78]. The cycle of infection that caused the BSE epidemic has been established through human intervention by the rendering of BSE-infected carcasses and feeding the produced meat and bone meal to cattle.…”

Prion and prion-like diseases in animals

“…Until today, no evidence of BSE infectivity in semen, embryos, placenta or milk (Bradley and Wilesmith, 1993;Buschmann and Groschup, 2005;Taylor et al, 1995;Wrathall et al, 2002) have been determined although increased risk of BSE development has been reported for the offspring of infected cows. The practice of feeding cattle with meat and bone meal (MBM) contaminated with infectious prions was proposed as the most likely responsible for the BSE epidemic and some hypotheses on the origin of BSE were considered: (i) the primary existence of sporadic or genetic BSE in cattle before its transmission via MBM Capobianco et al, 2007;Nicholson et al, 2008;Richt and Hall, 2008;Torres et al, 2013); (ii) sheep or goat-scrapie transmission to cattle through MBM (Hill et al, 1998); and (iii) human CJD (Colchester and Colchester, 2005).…”

Bovine spongiform encephalopathy

“…[104][105][106][107][108][109] Transmission via embryo transfer has also been investigated, but neither infected donor bulls nor infected donor cows were capable of transmitting BSE to recipient heifers or to the offspring. 110 Environmental contamination is not an important source of infection, nor is transmission by birds, ro-dents, or other vectors. 111,112 An epidemiologic review of the BSE prion-infected cattle born after the strict feed ban rules implemented in 1996 revealed that these cases did not have an increased likelihood of originating from UK herds with a high incidence of BSE in the past.…”